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膳食脂肪和大豆蛋白对大鼠氮杂丝氨酸诱导的胰腺癌发生及血浆胆囊收缩素的影响。

Effects of dietary fats and soybean protein on azaserine-induced pancreatic carcinogenesis and plasma cholecystokinin in the rat.

作者信息

Roebuck B D, Kaplita P V, Edwards B R, Praissman M

出版信息

Cancer Res. 1987 Mar 1;47(5):1333-8.

PMID:3815341
Abstract

Both dietary unsaturated fat and raw soybean products are known to enhance pancreatic carcinogenesis when fed during the postinitiation phase. A comparison of these two dietary components was made to evaluate the relative potency of each ingredient for enhancing pancreatic carcinogenesis and to determine if this enhancement was correlated with an increase in plasma cholecystokinin (CCK) levels. Male Wistar rats were initiated with a single dose of azaserine (30 mg/kg body weight) at 14 days of age. The rats were weaned to test diets formulated from purified ingredients. Dietary protein at 20% by weight was either casein or soy protein isolate (heat treated or raw). Corn oil was the unsaturated fat of major interest and it was fed at either 5 or 20% by weight. Pancreases were quantitatively evaluated for carcinogen-induced lesions at 2- and 4-month postinitiation. In a second experiment designed to closely mimic the above experiment, rats were implanted with cannulae which allowed plasma to be repetitively sampled over a 2.5-week period during which the test diets were fed. Plasma was collected both prior to introduction of the test diets and afterwards. Plasma CCK was measured by a specific radioimmunoassay. Both the 20% corn oil diet and the raw soy protein isolate diet enhanced pancreatic carcinogenesis. The effects of the raw soy protein isolate on the growth of the carcinogen-induced lesions were significantly greater than the effects of the 20% corn oil diet. Plasma CCK values were not elevated in the rats fed the 20% corn oil diet, but they were significantly elevated in the rats fed the raw soy protein isolate. Heat-treated soy protein isolate neither enhanced carcinogenesis nor elevated the plasma CCK level. This study demonstrates that certain plant proteins enhance the growth of carcinogen-induced pancreatic foci and that this effect is considerably greater than the enhancement by high levels of dietary unsaturated fat. Furthermore, the enhancement by the raw soy protein isolate may be mediated by CCK; but this does not appear to be the mechanism by which the unsaturated fat, corn oil, enhances pancreatic carcinogenesis.

摘要

已知在启动后阶段喂食时,膳食中的不饱和脂肪和生大豆制品都会增强胰腺癌的发生。对这两种膳食成分进行了比较,以评估每种成分增强胰腺癌发生的相对效力,并确定这种增强是否与血浆胆囊收缩素(CCK)水平的升高相关。雄性Wistar大鼠在14日龄时单次注射氮杂丝氨酸(30毫克/千克体重)进行启动。大鼠断奶后食用由纯化成分配制的试验饮食。按重量计20%的膳食蛋白质要么是酪蛋白,要么是大豆分离蛋白(热处理或生的)。玉米油是主要关注的不饱和脂肪,按重量计分别以5%或20%的比例喂食。在启动后2个月和4个月时,对胰腺中致癌物诱导的病变进行定量评估。在第二个旨在紧密模拟上述实验的实验中,给大鼠植入插管,以便在喂食试验饮食的2.5周期间重复采集血浆样本。在引入试验饮食之前和之后都采集血浆。通过特定的放射免疫测定法测量血浆CCK。20%玉米油饮食和生大豆分离蛋白饮食都增强了胰腺癌的发生。生大豆分离蛋白对致癌物诱导病变生长的影响明显大于20%玉米油饮食的影响。喂食20%玉米油饮食的大鼠血浆CCK值没有升高,但喂食生大豆分离蛋白的大鼠血浆CCK值明显升高。热处理的大豆分离蛋白既没有增强癌症发生,也没有提高血浆CCK水平。这项研究表明,某些植物蛋白会增强致癌物诱导的胰腺病灶的生长,而且这种作用比高水平膳食不饱和脂肪的增强作用要大得多。此外,生大豆分离蛋白的增强作用可能由CCK介导;但这似乎不是不饱和脂肪玉米油增强胰腺癌发生的机制。

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